Nonopioid Analgesics


Acetaminophen (paracetamol) is a first-line anti-pyretic and analgesic for mild to moderate pain for pediatric patients of all ages. Its popularity is highlighted by its wide therapeutic window, over-the-counter accessibility, lack of systemic effects, safety profile when given in appropriate doses, and opioid sparing effect when given for pediatric ambulatory surgery (Korpela et al. 1999). Although the exact anti-nociceptive mechanisms of acetaminophen continue to be elucidated, proposed explanations have included interference with seroton-ergic descending pain pathways (Anderson 2008) and the central inhibition of the enzyme cyclo-oxygenase (COX), thereby preventing the production of prostaglandins from arachi-donic acid. Prostaglandins are thought to play a role in nociceptive transmission by augmenting the release of excitatory neurotransmitters such as glutamate and substance P (Bjorkman et al. 1994, Choi et al. 2001) and blocking the release of inhibitory neurotransmitters (Ahmadi et al. 2002).

Acetaminophen may be given alone or in varying doses as a combination with codeine, oxycodone, or hydrocodone. When given alone, acetaminophen can be administered orally (multiple preparations), rectally or more recently, intravenously (mostly used outside the United States). Regardless of the route of administration, attention should be directed toward following acetaminophen dosing guidelines to avoid potential drug-induced toxicity (doses > 150 mg/kg or 10 times the recommended dose).

Following oral intake, acetaminophen plasma concentrations peak after 1-2 h with a reported half-life of 3-4 h. Recommended oral dose is 10-15 mg/kg q 4-6 h to a maximum dose of 50-75 mg/kg (Cranswick and Coghlan 2000). Rectal suppositories of acetaminophen, despite reported variability in absorption and pharmacokinetics (Anderson and Holford 1997), remain a popular means of drug delivery. Birmingham et al. (2001) recommended an initial dose of 40 mg/kg followed by 20 mg/kg doses every 6 h (Birmingham et al. 2001) based on a study age group of 3-12 years.

The use of intravenous acetaminophen in pediatric patients has increasingly garnered interest, with studies reporting predictable drug bioavailability (100%) and peak plasma concentrations occurring 1 h after injection (Anderson et al. 2005). However, given its relatively nascent and limited use in the United States, further studies are needed to clarify the role of IV acetaminophen in pediatric acute and chronic pain management.

Nonsteroidal Anti Inflammatory Drugs

Nonsteroidal anti inflammatory drugs (NSAIDs) are useful pharmacological agents for the treatment of mild to moderate pain and anti-pyrexia in the pediatric population. Their analgesic activity is thought to be due to the decrease in peripheral > central prostaglandin synthesis through the inhibition of the enzyme COX. Unlike acetaminophen which exhibits minimal peripheral side effects, prolonged NSAIDs use is associated with adverse complications including gastric wall thinning and ulceration, acute renal failure, and platelet dysfunction (Tobias 2000). Furthermore, the use of salicylates is thought to increase the risk of Reye's syndrome (characterized by acute hepatic failure and encephalopathy) and therefore not typically given for the treatment of fever or mild pain in pediatric patients exhibiting viral-like symptoms. NSAIDs may be administered orally, intravenously, intramuscularly, or rectally.


A phencyclidine derivative, ketamine, is well known for its dysphoria and dissociative anesthetic effects. Ketamine's analgesic properties are thought to be due to possible |x opioid activity (Finck and Ngai 1982, Smith et al. 1987) and NMDA receptor antagonism (Stubhaug et al. 1997, Stubhaug and Breivik 1997). Interest in ketamine has increased due to this latter activity as blockade of the NMDA receptor is thought to play a role in the development of central pain mechanisms such as "wind up" and hyperalgesia. Pediatric uses of ketamine include preoperative sedation, induction of general anesthesia, minimization of emergence delirium following general anesthesia, sedation/analgesia for invasive and non-invasive procedures (i.e., cardiac catheterization, wound dressing changes), and analgesic therapy for end-stage cancer pain (Abu-Shahwan and Chowdary 2007, Lois and De Kock 2008, Conway et al. 2009). Although ketamine causes minimal respiratory depression at sub-anesthetic doses, laryngospasm and hypersalivation are possible side effects (Green et al. 1998), with the latter effect being attenuated by the administration of an anti-cholinergic. Ketamine may be given intravenously, intramuscularly, or rectally.


Pediatric uses of clonidine (an a2-adrenergic agonist) include analgesic therapy (commonly as an adjunct to regional anesthesia) and treatment of preoperative anxiety (Mikawa et al. 1993, Ramesh et al. 1997, Bergendahl et al. 2004), postoperative nausea/vomiting (Handa and Fujii 2001), and emergence delirium (Kulka et al. 2001, Bock et al. 2002). Despite potential side effects of hypotension and bradycardia, clonidine is not associated with respiratory depression as seen with opioid analgesics. Clonidine may be administered by oral, rectal, or neuraxial (caudal, epidural) routes.

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